Aminoglycosides

Question 1

Aminoglycoside options

Answer 1

-Amikacin

-Gentamicin

Question 2

Gentamicin formulations

Answer 2

1. Gentocin- sterile injectable solution (IM, SC, IU but given IV off label)
2. Otomax, Mometamaxx
   -topical ointments for otitis externa
   -includes an antifungal
3. Topagen
   -topical spray for dermal lesions

Question 3

Amikacin formulations

Answer 3

1.Amiglyde-V
-sterile injectable solution
-labelled only for IU use in mares but often given off label IV in small animals and equine

**Generally more potent than Gentomicin.. but narrower spectrum of activity

Question 4

Neomycin

Answer 4

-various calf scour boluses, water soluble powders for food animals
-skin/ear ointments
-antimicrobial preservative in many vaccines

Question 5

Apramycin

Answer 5

-Apralan oral solution for swine scours caused by E. coli

Question 6

Aminoglycasides mechanism of action

Answer 6

Bind to bacterial ribosomal 30S subunit
-causes incorrect tRNA translation
-disrupts bacterial protein synthesis
-results in increased bacterial membrane permeability

Question 7

Factors allowing for aminogylcosides to access the bacteria

Answer 7

1. Need oxygen so very poor efficacy in anaerobic environment
2. Local pH
   -basic pH= aminoglycosides non ionized, easier to transport in but can diffuse out
   -acidic pH= Aminoglycosides more ionized, less transport in but then ion trapped
3. Purulent material in abscesses can inactivate aminoglycosides

Question 8

Aminoglycosides spectrum of activity

Answer 8

1. gram -
   -especially enteric bacteria (including pseudomonas)
2. Activity against staph spp
   -includes some MRSA/MRSP
3. Some activity against enterococcus, mycobacteria, mycoplasma

Question 9

What are aminoglycosides not effective against?

Answer 9

1. less activity against strep spp
   *especially amikacin
2. intracellular pathogens
   -including salmonella
3. Anaerobes

Question 10

Ways Aminoglycosides can become Resistance

Answer 10

1. Plasmid-mediated enzymes degrade aminoglycosides and prevent binding to ribosome 30S subunit
   **most important for determining clinical susceptibility
2. decreased permeability = adaptive resistance
3. Chromosomal resistance
   -changes to 30S binding sites so mutations don’t usually produce clinical resistance